It is now known that supersaturation can be produced in man and animals isothermally and isobarically by means of the counterdiffusion of gases of different diffusivities. This can promote more accurate calculations of actual supersaturations responsible for vascular bubbles which can be detected by doppler ultrasound. The objective of this proposal is to investigate: 1) cardiovascular and hematologic effects of vascular and tissue bubbles formed as a result of isobaric supersaturation due to counterdiffusion of inert gases having different diffusivity; 2) the opposite effect, and potential decompression advantage of isobaric undersaturation due to the opposite countertransport sequence. Because such conditions are without the hydrostatic pressure drop associated with decompression they are more suitable for determining the actual critical supersaturations causing bubbles to appear in the vasculature at different depths and/or saturation times. This information in turn is needed to design optimal decompression protocols. Existing assumptions in decompression theory and practice may then be tested against current knowledge of bubble formation and growth, and permissible supersaturations and saturation time may be more realistically related to ascent criteria. The controversial role of vascular bubbles as etiologic agents involved in the known hypovolemia and suspected endothelial damage of decompression sickness may then be investigated in the absence of decompression.